Universal measuring transducer for a multifunctional blood coagulation analyzer

1989 ◽  
Vol 23 (4) ◽  
pp. 128-131
Author(s):  
A. P. Dorokhov ◽  
A. A. Makeev ◽  
L. I. Shifrin
2015 ◽  
Vol 41 (03) ◽  
pp. 267-271 ◽  
Author(s):  
Satoshi Gando ◽  
Yuichi Ono ◽  
Asumi Mizugaki ◽  
Kenichi Katabami ◽  
Kunihiko Maekawa ◽  
...  

1999 ◽  
Vol 33 (1) ◽  
pp. 44-47
Author(s):  
N. A. Dobrovol'skii ◽  
P. R. Kostritso ◽  
T. A. Labinskaya ◽  
V. V. Makarov ◽  
A. S. Parfenov ◽  
...  

2019 ◽  
Vol 72 (7) ◽  
pp. 417-422
Author(s):  
Yohji IRIE ◽  
Hiroko YOSHIDA ◽  
Katsuyuki KAI ◽  
Yasushi MAKINO ◽  
Shinji SHIBATA ◽  
...  

2001 ◽  
Vol 5 (1) ◽  
pp. 70-73
Author(s):  
David Green
Keyword(s):  

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
B Engelmann ◽  
J Bischof ◽  
AL Dirk ◽  
N Friedrich ◽  
E Hammer ◽  
...  

2001 ◽  
Vol 21 (03) ◽  
pp. 82-96 ◽  
Author(s):  
D. Hoppensteadt ◽  
O. Iqbal ◽  
R. L. Bick ◽  
J. Fareed

SummaryThrombotic disorders are the most common cause of death in the United States. About two million individuals die each year from an arterial or venous thrombosis or related disorders. About 80% to 90% of all cases of thrombosis can now be defined with respect to cause. Of these, over 50% occur in patients who harbor a congenital or acquired blood coagulation protein or platelet defect which caused the thrombotic event. It is obviously of major importance to define those individuals harboring such a defect as this allows: 1) appropriate antithrombotic therapy to decrease risks of recurrence; 2) determination of the length of time the patient must remain on therapy for secondary prevention; and 3) allow for testing of family members of those harboring a blood coagulation protein or platelet defect which is hereditary (about 50% of all coagulation and platelet defects mentioned above). Aside from mortality, significant additional morbidity occurs from both arterial or venous thrombotic events, including, but not limited to paralysis (non-fatal thrombotic stroke), cardiac disability (repeated coronary events), loss of vision (retinal vascular thrombosis), fetal waste syndrome (placental vascular thrombosis), stasis ulcers and other manifestations of post-phlebitic syndrome, etc.


1974 ◽  
Vol 32 (01) ◽  
pp. 057-064 ◽  
Author(s):  
Y Nemerson ◽  
S.A Silverberg ◽  
J Jesty

SummaryTwo reactions of the extrinsic pathway of coagulation, the activations of Factor X and prothrombin, have been studied in purified systems and shown to be self-damping. Factor X was activated by the tissue factor - Factor VII complex, and prothrombin by two systems: the coagulant protein of Taipan venom, and the physiological complex of activated Factor X, Factor V, lipid, and calcium ions. In each case the yield of enzyme, activated Factor X or thrombin, is a function of the concentration of activator. These and other observations are considered as a basis for a control mechanism in coagulation.


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